- A herd of Friesian X Jersey cross-bred (FJXB) cows was used to look for genetic markers associated with mastitis resistance.
- A genetic marker has been identified that is associated with resistance to an intramammary challenge with Streptococcus uberis.
- Validation of the marker in a large, independent population will confirm the value of the marker for New Zealand dairy farmers.
- Genetic selection for mastitis resistance could result in significant financial benefits to dairy farmers.
Clinical mastitis (CM) can be identified in cows at milking time, but subclinical mastitis is much harder to detect. It relies on regular herd testing, the laborious process of testing every cow with a rapid mastitis test (RMT) or the expensive bacterial culturing of milk samples. Subclinical mastitis is dynamic; cows can self-cure and become re-infected between herd tests.
Subclinical infections affect milk production. For every doubling of the somatic cell count above 100,000 cells/mL, a cow loses 2% of her production2. Also, heifers infected with a Str. uberis intramammary infection (IMI) at calving have been shown to produce 7% less milk during their first 200 days in milk3. Cows that are genetically more resistant to mastitis would deliver substantial benefits to New Zealand dairy farmers.
The search for genetic markers
Identifying any component of the genetic basis of mastitis resistance involves using sophisticated tools and techniques, and collaborations between science organisations. A successful collaboration between LIC, ViaLactia Biosciences and DairyNZ enabled access to the phenotypic (observable characteristics) and genotypic (gene) information from the BoviQuest FJXB trial. Bioinformatic (analysis of biological data) investigations produced additional information on the associations between these data.
The BoviQuest FJXB Trial
The FJXB (Friesian X Jersey cross-bred) trial design allowed the discovery of genes and genetic variations responsible for economically important dairy traits. The FJXB F2 pedigree herd4, 5, was created by reciprocal crosses of Holstein-Friesian and Jersey animals to produce six F1 bulls of high genetic merit. Over two seasons, 864 F2 female progeny were produced through mating of high genetic merit F1 cows with the F1 bulls. Cows were managed on a single farm in Taranaki, under typical dairy farming practices using a seasonal, pasture-based system.
Collecting the phenotypes
To find genomic markers, phenotypes are measured and associated with mastitis occurrence or absence. Phenotypes measured in the FJXB cows included: incidence of clinical mastitis; prevalence of intramammary infections (measured four times during each of three successive lactations); and response to a Str. uberis challenge (once in their 3rd lactation).
Differences in cow response to the challenge with Streptococcus uberis were investigated following a single intramammary infusion of bacteria after a milking. Cows were monitored for mastitis for two weeks following challenge; when clinical mastitis was detected, cows were sampled and treated with antibiotics. Within seven days of the challenge, 71% of the herd had developed clinical mastitis.
How does a mastitis challenge study lead to a genomic marker?
Phenotypes collected from the FJXB cows were used to find regions of DNA associated with desirable traits, known as quantitative trait loci (QTL). Several QTL were found on different chromosomes. The most significant was associated with whether or not a cow developed clinical mastitis after the Str. uberis challenge. Using DNA from the six sires, genes in the QTL regions were tested for SNP (single nucleotide polymorphisms). A SNP is a single nucleotide difference in the DNA sequence, at a particular point in the gene, between paired chromosomes. SNP are important as they can be responsible for differences in gene function, in this case response to infection.
A total of 485 SNPs were identified in the sires for further investigation in the FJXB cows. The DNA of the FJXB cows was then sequenced to look for these SNP. When compared with the responses to challenge, one group of SNP in an area of one bovine chromosome was associated with ‘resistance’ to experimentally induced mammary infection (Littlejohn et al 2013).
The frequency of one particular SNP was compared with the infection rates in the cows. Cows can have either two copies of the ‘desirable’ version of the SNP (one on each paired chromosome), two copies of the ‘undesirable’ version or one of each. Having two copies of the ‘undesirable’ version of the SNP increased the likelihood of developing clinical mastitis under challenge conditions from 50% to over 80% (Table 1).
Could a genetic marker for mastitis be financially valuable?
Because large differences in the rate of clinical infection between cows carrying two different versions of the SNP were apparent, a basic economic prediction was carried out using the SmartSAMM gap calculator (smartsamm.co.nz), to determine if changes in the clinical mastitis rate would be financially valuable if achieved in normal farming practice.
Estimates suggest that reducing the incidence of CM from 15 cases to 10 cases per 100 cows (performance of median herds compared to top 25% of herds6) could lead to savings of around $500 per herd (for an average 390 cow herd) or $29.0 M for the New Zealand dairy industry.
It is now necessary to determine if cows that carry the more desirable version of the SNP respond similarly to natural infection and if the marker is important for sub-clinical infections. If it is, then another benefit could be a lower bulk milk somatic cell count (BMSCC) and an affect on milk yield.
Table 1: Association between single nucleotide polymorphism (SNP) versions and the response to an intramammary challenge with Str. uberis.
Version of SNP
% cows with clinical mastitis
2 ‘undesirable’ copies
1 ‘desirable’, 1 ‘undesirable’ copy
2 ‘desirable’ copies
So what’s next?
A marker of significant interest has been found in a population of FJXB cows, in response to an experimental mastitis challenge with Str. uberis. Investigation and validation of the marker in a large independent population is required before the marker can be considered for release to the dairy industry.
To achieve this, approximately 3000 heifers have been monitored and characterised during their first lactation since 2010. Enrolled to the study from a total of 11 herds, these heifers have been monitored for key phenotypic traits associated with mastitis resistance. Heifers provide the basis of the large independent population, as this ensures the validity of the mastitis historical data.
Additionally heifers were used as there was no influence of pre calving treatments (eg. teat sealants or dry cow therapy antibiotics) on the mastitis phenotype. Information on infection history (as assessed by routine milk sample collection for bacteriological analysis), production history (milk yields and composition) and other relevant data such as calving dates, treatment histories and breeding worth have been collected. To provide material for genotyping, blood samples were also collected from the heifers for DNA extraction.
During the 2013-2014 season, the DNA samples from the heifers are being genotyped for the marker discovered in the FJXB cows. Productivity, fertility, and survival traits will also be examined to determine if there are any negative traits associated with resistance to mastitis. This will help ensure that the markers are appropriate for use in breeding schemes to maximise lifetime productivity of dairy cows. A thorough financial analysis will be conducted if the validation of the genotypes in the heifers proves to be successful.
In future, the potential benefits may not only be derived from farmers ‘managing the cow right’. The whole industry may benefit from ‘breeding the right cows’ to reduce mastitis.
- Pearson, L.J., J.H. Williamson, S.J. Lacy-Hulbert, and J.E. Hillerton. 2010. Prevalance of Streptococcus uberis intramammary infection post-calving in a monozygotic twin cow herd. Page 120-125 in Mastitis Research into Practice, 5th IDF Mastitis Conference. Christchurch, New Zealand.
- Winkelman, A.M., W.A. Montgomerie, and D.L. Johnson. 2007. Effect of increased somatic cell count on lacttaion yields of milk, fat and protein. Proceedings of the New Zealand Society of Animal Production 67: 293-296.
- Pearson, L.J., J.H. Williamson, S.-A. Turner, S.J. Lacy-Hulbert, and J.E. Hillerton. 2013. Peripartum infection with Streptococcus uberis but not coagulase-negative staphylococci reduced milk production in primiparous cows. Journal of Dairy Science 96: 158-64.
- Spelman, R.J., F.M. Milllar, J.D. Hooper, M. Thielen, and D.J. Garrick. 2001. Experimental design for the QTL trial involving New Zealand Friesian and Jersey breeds. Page 393-396 in Proceedings of the Association for the Advancement of Animal Breeding and Genetics. Queenstown, New Zealand.
- Berry, S.D., N. Lopez-Villalobos, E.M. Beattie, S.R. Davis, L.F. Adams, N.L. Thomas, A.E. Ankersmit-Udy, A.M. Stanfield, K. Lehnert, H.E. Ward, J.A. Arias, R.J. Spelman, and R.G. Snell. 2010. Mapping a quantitative trait locus for the concentration of β-lactoglobulin in milk, and the effect of β-lactoglobulin genetic variants on the composition of milk from Holstein-Friesian x Jersey crossbred cows. New Zealand Veterinary Journal 58: 1-5.
- DairyNZ website - industry benchmarks
This article was originally published in Technical Series December 2013